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LRF promotes indirectly advantageous chromatin conformation via BGLT3-lncRNA expression and switch from fetal to adult hemoglobin

ABSTRACT: ChIP-seq for LRF/ZBTB7A in untransfected or LRF/ZBTB7A-overexpressing K562 cells, with or without hemin/EPO treatment and in K562 LRF/ZBTB7A-Knockdown cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE200135 | GEO | 2022/07/13

REPOSITORIES: GEO

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The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

Project description:Hemoglobinopathies, including sickle cell disease and _-thalassemia, are global public health concerns. Induction of fetal-type hemoglobin (HbF) is a promising means to treat these disorders; however, precisely how HbF expression is silenced in adult erythroid cells is not fully understood. Here, we show that the LRF/ZBTB7A transcription factor is a potent repressor of HbF production. LRF inactivation derepresses embryonic/fetal _-globin expression in mouse and human adult erythroid cells. We employed genome-wide analysis of the transcriptome, chromatin accessibility and LRF occupancy sites, and demonstrate that LRF occupies the _-globin loci and maintains nucleosome density necessary for _-globin silencing. LRF confers its repressive activity through a unique NuRD repressor complex independent of BCL11A. Strikingly, human erythroid lines lacking both LRF and BCL11A exhibited almost a complete switch in expression from adult- to fetal-type globin, suggesting that these two factors cumulatively represent the near entirety of _-globin repressive activity in adult erythroid cells. RNA-seq, LRF ChIP-seq and ATAC-seq assays were used to investigtae LRF binding, effect of LRF depletion on transcription and chromatin landscape in mouse and human cells.

2016-01-15 | E-GEOD-74977 | biostudies-arrayexpress

Expression data from control and LRF (leukemia/lymphoma related factor)-deficient mouse LT-HSCs

Project description:LRF, which is encoded by the ZBTB7A gene and formerly known as POKEMON (POK erythroid myeloid ontogenic factor), was originally identified as a PLZF (promyelocytic leukemia zinc finger) homologue interacting with BCL6 (B-cell lymphoma 6). LRF is a transcription factor that is broadly expressed in hematopoietic lineage cells, but its expression is particularly high in erythroblasts and germinal center (GC) B-cells. The goal of this study is to assess the effect of LRF loss on the LT-HSC transcriptome. Nine days after injection of adult mice with polyinosinic polycytidylic acid (pIpc) to activate Cre, total RNAs were isolated from double-sorted LT-HSCs from LRF Flox/+ Mx1-Cre+ and LRF Flox/Flox Mx1-Cre+ mice and processed for microarray analysis. We performed gene expression microarray analysis of FACS-sorted LT-HSCs (LSK IL7Ra-Flt3-CD150+CD48-) to assess the effect of Lrf loss on the LT-HSC transcriptome. Zbtb7a Flox/+ Mx1-Cre+ mice were used as a control to normalize the potential effects of Cre recombinase. LT-HSCs were FACS-sorted from three Lrf knockout (Zbtb7a Flox/Flox Mx1-Cre+) and two control (Zbtb7a Flox/+ Mx1-Cre+) mice, nine days after the first pIpC injection.

2012-10-26 | E-GEOD-41839 | biostudies-arrayexpress

The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

2016-01-15 | GSE74977 | GEO

Expression data from control and LRF (leukemia/lymphoma related factor)-deficient mouse LT-HSCs

2012-10-26 | GSE41839 | GEO

The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

Project description:The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

| PRJNA302116 | ENA

KLF1 directly activates expression of the novel fetal globin repressor, ZBTB7A/LRF, in erythroid cells

Project description:Genes encoding the human β-like hemoglobin proteins undergo a developmental switch from fetal γ-globin to adult β-globin expression at around the time of birth. β-hemoglobinopathies, such as sickle cell disease and β-thalassemia, result from mutations affecting the adult β-globin gene. The only treatment options currently available carry significant side-effects. Analyses of heritable variations in fetal hemoglobin (HbF) levels have provided evidence that reactivation of the silenced fetal γ-globin genes in adult erythroid cells is a promising therapy. The γ-globin repressor BCL11A has become the major focus with several studies investigating its regulation and function as a first step to inhibiting its expression or activity. However, a second repression mechanism has recently been shown to be mediated by the transcription factor ZBTB7A/LRF, suggesting that understanding the regulation of ZBTB7A may also be useful. Here we show that KLF1 directly drives expression of ZBTB7A in erythroid cells by binding to its proximal promoter. We have also uncovered an erythroid-specific regulation mechanism, leading to the upregulation of a novel ZBTB7A transcript in the erythroid compartment. The demonstration that ZBTB7A, like BCL11A, is a KLF1 target gene also fits with the observation that reduced KLF1 expression or activity is associated with HbF derepression.

2017-04-13 | GSE97671 | GEO

LRF promotes indirectly advantageous chromatin conformation via BGLT3-lncRNA expression and switch from fetal to adult hemoglobin

Project description:LRF promotes indirectly advantageous chromatin conformation via BGLT3-lncRNA expression and switch from fetal to adult hemoglobin

| PRJNA823042 | ENA

Transcription factor ZBTB7A-deficiency effect on U87MG cells in vitro

Project description:Analysis of glioblastoma cell line U87MG depleted for ZBTB7A (Zinc Finger and BTB Domain Containing 7A, also known as FBI1, POKEMON or LRF). ZBTB7A is transcription factor that represses the transcription of a wide range of genes involved in cell proliferation and differentiation. Results provide insight into the role of ZBTB7A in glioblastoma.

2023-02-08 | GSE196320 | GEO

LRF genome-wide occupancy in CD4+ T cells

Project description:To examine whether LRF protein could bind cis-regulatory elements in the genes that LRF regulates. We performed Chromatin immunoprecipitation followed by deep-sequencing (ChIPseq) on activated T cells using an in vivo biotinylation and streptavidin pull-down approach.

2022-03-30 | GSE149993 | GEO

Expression data from control and LRF-deficient mouse germinal center B cells

Project description:B cells are indispensable for humoral immunity, as they ultimately give rise to antibody-secreting plasma cells. During T cell-dependent antibody responses, naive B cells form germinal centers (GCs), a distinct histologic structure found in secondary lymphoid organs. Naive B cells become activated upon interaction with T cells and antigen presenting cells, and begin to rapidly proliferate and form the characteristic GC structure. To elucidate the overall effect of LRF loss in the GCB cell transcriptome, gene expression microarray analysis of FACS-sorted GCB cells was performed. LRF Flox/+ mb-1 Cre+ mice were used as a control to normalize the potential effects of Cre recombinase, and four RNA samples for each genotype were used for the analysis. B cell-specific LRF knockout (LRF Flox/Flox mb-1 Cre+) and control (LRF Flox/+ mb-1 Cre+) mice (4 each) were immunized with sheep red blood cells, and GCB cells were FACS-sorted 7 days later.

2011-04-08 | E-GEOD-28449 | biostudies-arrayexpress

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